The effects of caveolin1 on Î² cell proliferation

Li, Haicheng; Peng, Hangya; Xu, Haixia; Xu, Fen; Lin, Shuo; Kh, Lin; Zeng, Wen

doi:10.14715/cmb/2018.64.1.8

Cited by 4 publications

(2 citation statements)

References 25 publications

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“…To date, several studies have reported that CAV1 induces sensitization to cell death in beta cells [ 53 , 54 , 55 ]. An association between CAV1 and MAPKs has been reported in various cell types.…”

Section: Discussionmentioning

confidence: 99%

Loss of Caveolin-1 Is Associated with a Decrease in Beta Cell Death in Mice on a High Fat Diet

Urzúa

Murillo

Castro-Sepúlveda

et al. 2020

IJMS

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Elevated free fatty acids (FFAs) impair beta cell function and reduce beta cell mass as a consequence of the lipotoxicity that occurs in type 2 diabetes (T2D). We previously reported that the membrane protein caveolin-1 (CAV1) sensitizes to palmitate-induced apoptosis in the beta pancreatic cell line MIN6. Thus, our hypothesis was that CAV1 knock-out (CAV1 KO) mice subjected to a high fat diet (HFD) should suffer less damage to beta cells than wild type (WT) mice. Here, we evaluated the in vivo response of beta cells in the pancreatic islets of 8-week-old C57Bl/6J CAV1 KO mice subjected to a control diet (CD, 14% kcal fat) or a HFD (60% kcal fat) for 12 weeks. We observed that CAV1 KO mice were resistant to weight gain when on HFD, although they had high serum cholesterol and FFA levels, impaired glucose tolerance and were insulin resistant. Some of these alterations were also observed in mice on CD. Interestingly, KO mice fed with HFD showed an adaptive response of the pancreatic beta cells and exhibited a significant decrease in beta cell apoptosis in their islets compared to WT mice. These in vivo results suggest that although the CAV1 KO mice are metabolically unhealthy, they adapt better to a HFD than WT mice. To shed light on the possible signaling pathway(s) involved, MIN6 murine beta cells expressing (MIN6 CAV) or not expressing (MIN6 Mock) CAV1 were incubated with the saturated fatty acid palmitate in the presence of mitogen-activated protein kinase inhibitors. Western blot analysis revealed that CAV1 enhanced palmitate-induced JNK, p38 and ERK phosphorylation in MIN6 CAV1 cells. Moreover, all the MAPK inhibitors partially restored MIN6 viability, but the effect was most notable with the ERK inhibitor. In conclusion, our results suggest that CAV1 KO mice adapted better to a HFD despite their altered metabolic state and that this may at least in part be due to reduced beta cell damage. Moreover, they indicate that the ability of CAV1 to increase sensitivity to FFAs may be mediated by MAPK and particularly ERK activation.

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Section: Discussionmentioning

confidence: 99%

Loss of Caveolin-1 Is Associated with a Decrease in Beta Cell Death in Mice on a High Fat Diet

Urzúa

Murillo

Castro-Sepúlveda

et al. 2020

IJMS

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“…The Caveolin 1 levels decreased in mesenteric vascular smooth muscle cell from type 2 diabetic Goto-Kakizaki rats [23]. Besides, Caveolin 1 was also mediates β-cell apoptosis and proliferation [24], implying that Caveolin 1 may inhibit the development of diabetes. In the heart tissue of rat models of abdominal aortic constriction constructed left ventricular hypertrophy, the levels of Caveolin 1 decreased along with the increase of apelin receptor (APJ).…”

Section: Introductionmentioning

confidence: 93%

Caveolin 1 Reduces High Glucose-Induced Hypertrophy and Inflammatory Fibrosis of H9C2 Cardiomyocytes By Inhibiting NF-κB Signaling

Gong

Yuan

Luo

et al. 2021

Preprint

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Background: Cardiac hypertrophy and inflammatory fibrosis are the basic pathological changes of the prevalent microvascular diabetes complication known as diabetic cardiomyopathy (DCM). Previous studies of the Caveolin 1 protein and the lipid raft structures known as caveolae—small invaginations of the plasma membranes of certain cell types (including cardiomyocytes)—have linked this protein to fat metabolism disorders, inflammation, diabetes, and cardiovascular disease. However, there are no reports linking Caveolin 1 to DCM. Here, we show that Caveolin 1 plays a vital role in the hypertrophy and inflammatory fibrosis of H9C2 cardiomyocytes induced by high glucose (HG) via inhibiting the NF-κB signaling.Methods: The H9C2 cardiomyocytes induced by HG were used as the experimental model in this study to explicit the effect of Caveolin 1 on DCM and the underlying mechanisms involved. Unpaired Student’s t test was used for comparison between two groups. For multiple comparisons, data were analyzed by one-way ANOVA with Bonferroni post hoc test multiple comparisons.Results: (1) Exposure of H9C2 cardiomyocytes to HG activated NF-κB signaling and induced the expression of downstream NF-κB target genes including both hypertrophic factors and inflammatory fibrosis factors; (2) Intriguingly, exposure of cardiomyocytes to HG led to decreased Caveolin 1 levels, and this decrease occurred in an HG-exposure-time-dependent manner; (3) Overexpression of Caveolin 1 reduces phosphorylation of p65 and blocks the nuclear accumulation of this NF-κB component in HG-exposed cardiomyocytes, and inhibits transcriptional activation of NF-κB target genes; (4) Knocking down Caveolin 1 exacerbates the HG-induced promotion of the aforementioned NF-κB hypertrophic factors and inflammatory fibrosis factors, all of which have been linked to DCM pathogenesis. Conclusions: Our study supports that Caveolin 1 can protect against hypertrophy and inflammatory fibrosis induced by HG, specifically by suppressing NF-κB signaling activity. Accordingly, some medical implications of our study include that i) Caveolin 1 may protect against the development of DCM and ii) may represent a target for developing therapeutics to protect against this highly prevalent and dangerous microvascular complications of diabetes.

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Caveolin-1 deficiency alleviates palmitate-induced intracellular lipid accumulation and inflammation in pancreatic β cells

Zeng,

Cai,

Liu

et al. 2023

J Physiol Biochem

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The effects of caveolin1 on Î² cell proliferation

Cited by 4 publications

References 25 publications

Loss of Caveolin-1 Is Associated with a Decrease in Beta Cell Death in Mice on a High Fat Diet

Loss of Caveolin-1 Is Associated with a Decrease in Beta Cell Death in Mice on a High Fat Diet

Caveolin 1 Reduces High Glucose-Induced Hypertrophy and Inflammatory Fibrosis of H9C2 Cardiomyocytes By Inhibiting NF-κB Signaling

Caveolin-1 deficiency alleviates palmitate-induced intracellular lipid accumulation and inflammation in pancreatic β cells

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